AKT primes snail‐induced EMT concomitantly with the collective migration of squamous cell carcinoma cells

Okui, Gaku; Tobiume, Kei; Rizqiawan, Andra; Yamamoto, Kazuhiro; Shigeishi, Hideo; Ono, Shigehiro; Higashikawa, Koichiro; Kamata, Nobuyuki

doi:10.1002/jcb.24545

Cited by 19 publications

(18 citation statements)

References 24 publications

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“…The phospho-AKT level is a classic indicator to evaluate AKT activity (40). Okui et al demonstrated that the PI3K/AKT signaling pathway is closely associated with EMT induction and human tumor development (41). In the present study, IL-8 stimulation could noticeably enhance the phosphorylated AKT levels as well as the motility and invasiveness of RCC cells.…”

Section: Discussionsupporting

confidence: 55%

IL-8 induces the epithelial-mesenchymal transition of renal cell carcinoma cells through the activation of AKT signaling

Zhou

Liu

et al. 2016

Oncology Letters

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Abstract. The epithelial-mesenchymal transition (EMT) process has increasingly been examined due to its role in the progression of human tumors. Renal cell carcinoma (RCC) is one of the most common urological tumors that results in patient mortality. Previous studies have demonstrated that the EMT process is closely associated with the metastasis of RCC; however, the underlying molecular mechanism has not been determined yet. The present study revealed that interleukin (IL)-8 was highly expressed in metastatic RCC. IL-8 could induce the EMT of an RCC cell line by enhancing N-cadherin expression and decreasing E-cadherin expression. Furthermore, IL-8 could induce AKT phosphorylation, and the phosphatidylinositol-4,5-bisphosphate 3-kinase inhibitor LY294002 could inhibit the EMT of RCC cells that was induced by IL-8. Therefore, these results suggest that IL-8 is able to promote the EMT of RCC through the activation of the AKT signal transduction pathway, and this may provide a possible molecular mechanism for RCC metastasis.

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Section: Discussionsupporting

confidence: 55%

IL-8 induces the epithelial-mesenchymal transition of renal cell carcinoma cells through the activation of AKT signaling

Zhou

Liu

et al. 2016

Oncology Letters

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“…It has also been reported that Akt, which acts downstream of PI3K, is very important for upregulation of Slug and Twist, two transcriptional factors that initiate EMT. 33 Previously, Severson et al 34 showed that JAM-A dimerization promotes Ras-proximate-1 (Rap1)-GTPase activation, beta 1 integrin upregulation and enhances cell migration, one of the hallmarks of EMT. Mandell et al 35 confirmed that JAM-A regulates epithelial cell morphology by modulating the activity of the Rap1-GTPase.…”

Section: Jam-a a Member Of The Junctional Adhesion Molecule Family mentioning

confidence: 99%

High expression of junctional adhesion molecule-A is associated with poor survival in patients with epithelial ovarian cancer

et al. 2019

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Purpose: Aberrant expression of different tight junction proteins, including the junctional adhesion molecule-A (JAM-A), has been frequently reported in association with tumor progression of several malignancies. To our knowledge, this is the first study examining the clinical significance of JAM-A gene expression in epithelial ovarian cancer. Methods: JAM-A expression levels in 44 epithelial ovarian cancer and 12 benign formalin-fixed paraffin-embedded samples were determined by reverse transcription quantitative polymerase chain reaction. Receiver operating characteristic (ROC) curve analysis was used to determine the diagnostic and prognostic potential of JAM-A. Associations between JAM-A expression and clinicopathological characteristics of epithelial ovarian cancer were analyzed using Fisher’s exact test. The Kaplan–Meier method and univariate Cox regression analysis were used for the survival analysis. P ⩽ 0.05 was considered statistically significant. Results: ROC curve analyses showed that JAM-A gene expression exhibits both diagnostic and prognostic performance in epithelial ovarian cancer (area under the curve (AUC) 0.640, 95% confidence interval (CI) 0.488, 0.792, sensitivity 43.18%, specificity 100% and AUC 0.621, 95% CI 0.427, 0.816, sensitivity 52.63%, specificity 85%, respectively). JAM-A expression was significantly associated with International Federation of Gynecologists and Obstetricians (FIGO) stage ( P =0.049) and the Kaplan–Meier method demonstrated that patients with high expression of JAM-A had significantly worse overall survival compared to patients with low JAM-A expression ( P =0.004). Moreover, univariate Cox regression analysis showed that FIGO stage, peritoneal metastasis, residual tumor and JAM-A expression were significantly associated with reduced overall survival in epithelial ovarian cancer. Conclusions: Our results indicate that high levels of JAM-A expression are associated with an advanced clinicopathological feature and may have diagnostic potential; also, it could be a predictor of poor overall survival in patients with epithelial ovarian cancer.

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“…Cell cycle is verified to be modulated by many cell-cycle promotors and inhibitors, such as Rb and cyclin D1 in the regulation of the G1/S transition. 39 , 40 Compared with the NC-transfected cells, the protein and mRNA expressions of p21 Cip1 and p27 Kip1 , 2 cell-cycle inhibitors, were increased in miR-495-transfected cells. However, the expression of cyclin D1, a cell-cycle promoter, was decreased in miR-495-transfected cells.…”

Section: Resultsmentioning

confidence: 98%

Downregulated miR-495 Inhibits the G1-S Phase Transition by Targeting Bmi-1 in Breast Cancer

Wang

Liu

et al. 2015

Medicine

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AKT primes snail‐induced EMT concomitantly with the collective migration of squamous cell carcinoma cells

Cited by 19 publications

References 24 publications

IL-8 induces the epithelial-mesenchymal transition of renal cell carcinoma cells through the activation of AKT signaling

IL-8 induces the epithelial-mesenchymal transition of renal cell carcinoma cells through the activation of AKT signaling

High expression of junctional adhesion molecule-A is associated with poor survival in patients with epithelial ovarian cancer

Downregulated miR-495 Inhibits the G1-S Phase Transition by Targeting Bmi-1 in Breast Cancer

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